Sudden infant death syndrome (SIDS) occurs during a sleep epoch in infants 1-6 months of age and is a major cause of infant mortality in the United States. Because SIDS occurs in infants primarily during periods of sleep, maturational and vigilance-related alterations in cardiopulmonary homeostasis and arousability are implicated in the pathogenesis of SIDS. Although the cause of SIDS is not known, it is likely to be a multifactorial disease. Pathological and epidemiological findings have suggested roles for mild respiratory infections, chronic hypoxia, and other factors that are known to alter arousability from sleep in adults and neonates. The specific aim of this proposal is to develop an animal model for the study of environmental and physiological factors implicated in the pathogenesis of SIDS. Such a model is currently not available. The proposed model will use the neonatal cat, which is a classically-used species for the study of both sleep and respiration. The proposed experiments will determine whether arousal from sleep in response to an auditory stimulus is impaired in kittens undergoing respiratory tract infections. At 14 or 28 days of age, kittens will be chronically implanted with electrodes for recording EEG and EMG. Following a baseline evaluation of sleep, kittens will be inoculated intranasally with feline herpes virus to induce respiratory tract infection. Sleep will then be monitored for up to 2 weeks. Arousal in response to auditory stimuli will be determined as a function of time postinoculation and circadian period. Control animals will be similarly evaluated after intranasal inoculation with heat-killed virus. The proposed experiments invoke the study of infectious disease as a representative example of a SIDS risk factor that could be studied using this model. The model could similarly be applied to other SIDS risk factors and their potential interactions. Furthermore, simple alterations in the behavioral testing chambers could permit the evaluation of arousal in response to hypoxia. The development of such a model is critical to eventually understanding the role of environmental and physiological perturbations in precipitating SIDS in infants, and to developing effective strategies for the prevention of SIDS.